Prostaglandins have been demonstrated to affect basal and hormonal stimulated bile flow in several species, to change cyclic AMP secretory rates in bile, and to be quantitatively present in relatively large amounts in hepatic bile. The physiologic role of the prostaglandins in hepatic bile flow remains undetermined. Evaluation of the effects of the more recently identified prostaglandins, prostacyclin and its stable breakdown product 6 keto PGF2alpha and thromboxane, may disclose new information concerning the role of these agents in bile flow as well as their mechanism of action. The increased information produced by these studies may indicate a mediator role for the prostaglandins in membrane mechanisms controlling basal and hormonal stimulated bile flow. The role of the prostaglandins in gallbladder function has been extensively evaluated in animals. Muscular gallbladder contraction and mucosal water transport are altered by the prostaglandins. These functions may play an important role in the symptoms and pathologic findings in actue and chronic cholecystitis. The importance of the prostaglandins as mediators of inflammation in other systems suggests that they may play a role in mediating the common inflammatory condition of cholecystitis. Preliminary research has disclosed significant prostaglandin metabolism in gallbladder tissue, making it possible to critically evaluate the role of the prostaglandins in gallbladder inflammation as well as any effect these pervasive substances may have on biliary colic and gallbladder mucosal absorptive capacity in cholecystitis. The systematic study of prostaglandin metabolism in animal models of cholecystitis will be followed by a determination of the effects of prostaglandin synthetase inhibitors on the pathologic process and prostaglandin synthesis. These studies will demonstrate the agent and dose of prostaglandin synthetase inhibitor to be evaluated in determining the effects of these substances on pain, inflammation and prostaglandin metabolism in human acute and chronic cholecystitis. These studies may define a chemical mediator of the symptoms of cholecystitis and identify methods to alter its metabolism.